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The evolution of trauma care is driven by a synergistic relationship between civilian and military medical systems. Although the characteristics of civilian injuries differ from those encountered on the battlefield, the pathophysiologic process of dying is the same and dominated by exsanguination and central nervous trauma. As such, therapies that interfere with the physiologic ability to compensate hemorrhage may play a key role to buy time until hemostatic surgery can be initiated. From a variety of remedies with the potential to prolong the compensation phase or to reverse the decompensation phase of shock, arginine vasopressin (AVP) is one of the most promising and best-evaluated drugs. Animal studies and various case report series provide some evidence that AVP may improve blood pressure even when conventional therapies fail, thus preventing hypovolemic cardiac arrest and enabling resuscitation from fatal hemorrhage. On the basis of this civilian experience, it seems reasonable to consider AVP for hypotensive resuscitation in the austere, resource-constrained battlefield environment. However, the significance of AVP as a rescue medication for life-threatening hemorrhage has yet to be proven.

Unlabelled: In a porcine model of uncontrolled hemorrhagic shock, we evaluated the effects of vasopressin versus an equal volume of saline placebo versus fluid resuscitation on hemodynamic variables and short-term survival. Twenty-one anesthetized pigs were subjected to severe liver injury. When mean arterial blood pressure was <20 mm Hg and heart rate decreased, pigs randomly received either vasopressin IV (0.4 U/kg; n = 7), an equal volume of saline placebo (n = 7), or fluid resuscitation (1000 mL each of lactated Ringer's solution and hetastarch; n = 7). Thirty minutes after intervention, surviving pigs were fluid resuscitated while bleeding was surgically controlled. Mean (+/- SEM) arterial blood pressure 5 min after the intervention was significantly (P < 0.05) higher after vasopressin than with saline placebo or fluid resuscitation (58 +/- 9 versus 7 +/- 3 versus 32 +/- 6 mm Hg, respectively). Vasopressin improved abdominal organ blood flow but did not cause further blood loss (vasopressin versus saline placebo versus fluid resuscitation 10 min after intervention, 1343 +/- 60 versus 1350 +/- 22 versus 2536 +/- 93 mL, respectively; P < 0.01). Seven of 7 vasopressin pigs survived until bleeding was controlled and 60 min thereafter, whereas 7 of 7 saline placebo and 7 of 7 fluid resuscitation pigs died (P < 0.01). We conclude that vasopressin, but not saline placebo or fluid resuscitation, significantly improves short-term survival during uncontrolled hemorrhagic shock., Implications: Although IV fluid administration is the mainstay of nonsurgical management of trauma patients with uncontrolled hemorrhagic shock, the efficacy of this strategy has been discussed controversially. In this animal model of severe liver trauma with uncontrolled hemorrhagic shock, vasopressin, but not saline placebo or fluid resuscitation, improved short-term survival.

When ventilating an unintubated patient with a standard adult self-inflating bag, high peak inspiratory flow rates may result in high peak airway pressures with subsequent stomach inflation. In a previous study we have tested a newly developed mouth-to-bag-resuscitator (max. volume, 1500 ml) that limits peak inspiratory flow, but the possible advantages were masked by excessive tidal volumes. The mouth-to-bag-resuscitator requires blowing up a balloon inside the self-inflating bag that subsequently displaces air, which then flows into the patient's airway. Due to this mechanism, gas flow and peak airway pressures are reduced during inspiration when compared with a standard bag-valve-mask-device. In addition, the device allows the rescuer to use two hands instead of one to seal the mask on the patient's face. The purpose of the present study was to assess the effects of the mouth-to-bag-resuscitator, which was modified to produce a maximum tidal volume of 500 ml, compared with a paediatric self-inflating bag (max. volume, 380 ml), and a standard adult self-inflating bag (max. volume, 1500 ml) in an established bench model simulating an unintubated patient with respiratory arrest. The bench model consisted of a face mask, manikin head, training lung (lung compliance, 100 ml/0.098 kPa (100ml/cm H2O); airway resistance, 0.39 kPa/(l s) (4 cm H2O/(l s)), and a valve simulating lower oesophageal sphincter pressure, 1.47 kPa (15 cm H2O). Twenty critical care nurses volunteered for the study and ventilated the manikin for 1 min with a respiratory rate of 20 min(-1) with each ventilation device in random order. The mouth-to-bag-resuscitator versus paediatric self-inflating bag resulted in significantly (P < 0.05) higher lung tidal volumes (302 +/- 41 ml versus 233 +/- 22 ml), and peak airway pressure (10 +/- 1 cm H2O versus 9 +/- 1 cm H2O), but comparable inspiratory time fraction (28 +/- 5% versus 27 +/- 5%, Ti/Ttot), peak inspiratory flow rate (0.6 +/- .01 l/s versus 0.6 +/- 0.2 l/s), and stomach inflation (149 +/- 495 ml/min versus 128 +/- 278 ml/min). In comparison with the adult self-inflating bag, there was significantly (P < 0.05) less gastric inflation (3943 +/- 4896 ml/min versus 149 +/- 495 ml/min versus 128 +/- 278 ml/min, respectively) with both devices, but the standard adult self-inflating bag had significantly higher lung tidal volumes (566 +/- 77 ml), peak airway pressure (13 +/- 1 cm H2O), and peak inspiratory flow rate (0.8 +/- 0.11 l/s). In conclusion, comparing the mouth-to-bag-resuscitator with small tidal volumes versus the paediatric self-inflating-bag during simulated ventilation of an unintubated patient in respiratory arrest resulted in comparable marginal stomach inflation, but significantly reduced the likelihood of gastric inflation compared to the adult self-inflating-bag. Lung tidal volumes were improved from approximately 250 ml with the paediatric self-inflating-bag to approximately 300 ml with the mouth-to-bag-resuscitator.

Objective: Mechanical circulatory support can maintain vital organ perfusion in patients with cardiac failure unresponsive to standard pharmacologic treatment. The purpose of the current study was to report complication and survival rates in patients supported with emergency percutaneous venoarterial cardiopulmonary bypass because of prolonged cardiogenic shock or cardiopulmonary arrest., Design: Retrospective clinical study., Subjects: A total of 46 patients supported with venoarterial cardiopulmonary bypass, 25 because of cardiogenic shock unresponsive to pharmacologic therapy and 21 because of cardiopulmonary arrest unresponsive to standard advanced cardiac life support., Results: In 41 of the 46 patients (89%), stable extracorporeal circulation was established; in five patients (11%), femoral cannulation was accomplished only after a surgical cutdown. A total of 28 patients were weaned from cardiopulmonary bypass (19 of 25 patients with cardiogenic shock vs. 9 of 21 patients with cardiopulmonary arrest, p =.03), and 13 patients had long-term survival (10 of 25 patients with cardiogenic shock vs. 3 of 21 patients with cardiopulmonary arrest, p =.1). Complications directly related to the use of cardiopulmonary bypass were found in 18 patients (39%), major complications related to femoral cannulation being the most common single cause for bypass-associated morbidity (eight patients, 17%)., Conclusions: Long-term survival rates after emergency percutaneous cardiopulmonary bypass are encouraging in patients with an underlying cardiocirculatory disease amenable to immediate corrective intervention (angioplasty, surgery, transplantation).

Background: The authors compared the effects of vasopressin fluid resuscitation on survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs., Methods: A midline laparotomy was performed on 23 domestic pigs, followed by an incision, and subsequent finger fraction across the right medial liver lobe. During hemorrhagic shock, animals were randomly assigned to receive either 0.4 U/kg vasopressin (n = 9), or fluid resuscitation (n = 7), or saline placebo (n = 7), respectively. A continuous infusion of 0.08 U x kg(-1) x min(-1) vasopressin in the vasopressin group, or normal saline was subsequently administered in the fluid resuscitation and saline placebo group, respectively. After 30 min of experimental therapy, bleeding was controlled by surgical intervention, and blood transfusion and rapid fluid infusion were subsequently performed., Results: Maximum mean arterial blood pressure during experimental therapy in the vasopressin-treated animals was significantly higher than in the fluid resuscitation and saline placebo groups (mean +/- SD, 72 +/- 26 vs 38 +/- 16 vs 11 +/- 7 mmHg, respectively; P< 0.05). Subsequently, mean arterial blood pressure remained at approximately 40 mmHg in all vasopressin-treated animals, whereas mean arterial blood pressure in all fluid resuscitation and saline placebo pigs was close to aortic hydrostatic pressure (approximately 15 mmHg) within approximately 20 min of experimental therapy initiation. Total blood loss was significantly higher in the fluid resuscitation pigs compared with vasopressin or saline placebo after 10 min of experimental therapy (65 +/- 6 vs 42 +/- 4 vs 43 +/- 6 ml/kg, respectively; P< 0.05). Seven of seven fluid resuscitation, and seven of seven saline placebo pigs died within approximately 20 min of experimental therapy, while 8 of 9 vasopressin animals survived more than 7 days (P < 0.05)., Conclusions: Vasopressin, but not fluid resuscitation or saline placebo, ensured survival with full recovery in this liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.

The fear of acquiring infectious diseases has resulted in reluctance among healthcare professionals and the lay public to perform mouth-to-mouth ventilation. However, the benefit of basic life support for a patient in cardiopulmonary or respiratory arrest greatly outweighs the risk for secondary infection in the rescuer or the patient. The distribution of ventilation volume between lungs and stomach in the unprotected airway depends on patient variables such as lower oesophageal sphincter pressure, airway resistance and respiratory system compliance, and the technique applied while performing basic or advanced airway support, such as head position, inflation flow rate and time, which determine upper airway pressure. The combination of these variables determines gas distribution between the lungs and the oesophagus and subsequently, the stomach. During bag-valve-mask ventilation of patients in respiratory or cardiac arrest with oxygen supplementation (> or = 40% oxygen), a tidal volume of 6-7 ml kg(-1) ( approximately 500 ml) given over 1-2 s until the chest rises is recommended. For bag-valve-mask ventilation with room-air, a tidal volume of 10 ml kg(-1) (700-1000 ml) in an adult given over 2 s until the chest rises clearly is recommended. During mouth-to-mouth ventilation, a breath over 2 s sufficient to make the chest rise clearly (a tidal volume of approximately 10 ml kg(-1) approximately 700-1000 ml in an adult) is recommended.

Background: Studies in animals have suggested that intravenous vasopressin is associated with better vital-organ perfusion and resuscitation rates than is epinephrine in the treatment of cardiac arrest. We did a randomised comparison of vasopressin with epinephrine in patients with ventricular fibrillation in out-of-hospital cardiac arrest., Methods: 40 patients in ventricular fibrillation resistant to electrical defibrillation were prospectively and randomly assigned epinephrine (1 mg intravenously; n = 20) or vasopressin (40 U intravenously; n = 20) as primary drug therapy for cardiac arrest. The endpoints of this double blind study were successful resuscitation (hospital admission), survival for 24 h, survival to hospital discharge and neurological outcome (Glasgow coma scale). Analyses were by intention to treat., Findings: Seven (35%) patients in the epinephrine group and 14 (70%) in the vasopressin group survived to hospital admission (p = 0.06). At 24 h, four (20%) epinephrine-treated patients and 12 (60%) vasopressin-treated patients were alive (p = 0.02). Three (15%) patients in the epinephrine group and eight (40%) in the vasopressin group survived to hospital discharge (p = 0.16). Neurological outcomes were similar (mean Glasgow coma score at hospital discharge 10.7 [SE 3.8] vs 11.7 [1.6], p = 0.78)., Interpretation: In this preliminary study, a significantly larger proportion of patients created with vasopressin than of those treated with epinephrine were resuscitated successfully from out-of-hospital ventricular fibrillation and survived for 24 h. Based upon these findings, larger multicentre studies of vasopressin in the treatment of cardiac arrest are needed.

New results in the area of mechanical cardiopulmonary resuscitation indicate that during external cardiac massage, the blood flow is achieved both by direct cardiac compression and a generalized increase in the intrathoracic pressure. While, in accordance with the classical theory, the heart is compressed between the sternum and the vertebral column, the thoracic pump mechanism requires a consideration of all blood-carrying structures within the thorax as elastic tubes or chambers that are capable of being compressed by externally administered pressure. Only such variations of the technique presently used may be of benefit which can be achieved with simple adjuncts and which have a positive effect on both mechanisms of blood flow.

Sixty-eight adults with cardiac arrest (asystole and electromechanical dissociation) were randomly allocated for treatment with standard (1 mg) or high-dose epinephrine (5 mg). If the first dose of adrenaline (1 or 5 mg) failed, standardized advanced life-support was applied in all cases. High-dose adrenaline was associated with higher initial resuscitation success rates (16 of 28) than standard-dose adrenaline (6 of 40), whereas hospital discharge rates were not significantly different between the groups. Blood pressure was significantly higher in the high-dose adrenaline group in comparison to the standard dose at 1 and 5 min after resuscitation. Although high-dose adrenaline appears to improve cardiac resuscitation success, the duration of global cerebral ischaemia seems to determine the ultimate outcome.

During cardiopulmonary resuscitation (CPR), arterial pH and carbon dioxide tension (PCO2) do not reflect the marked acidosis and hypercapnia seen in venous blood samples during CPR. Epinephrine causes an increase in myocardial and cerebral blood flow during CPR, but the influence on regional venous PCO2 and pH is as yet unknown. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45 micrograms/kg epinephrine (n = 7) after 5 min of ventricular fibrillation and 3 min of open-chest CPR. Blood samples were obtained during CPR from the aorta, pulmonary artery, great cardiac vein, and sagittal sinus before and 90 s and 5 min after drug administration. Regional blood flow was measured with tracer microspheres. Plasma catecholamines were quantified by high-performance liquid chromatography in arterial blood. PCO2 90 s after drug administration in arterial, mixed venous, myocardial venous, and cerebral venous blood were (means +/- SD) 36 +/- 8, 67 +/- 9, 74 +/- 14, and 79 +/- 19 mmHg in the control group and 35 +/- 11, 62 +/- 12, 73 +/- 10, and 71 +/- 14 mmHg in the epinephrine group. pH values 90 s after drug administration in the same blood samples were 7.29 +/- 0.11, 7.11 +/- 0.09, 7.04 +/- 0.09, and 7.07 +/- 0.10 in the control group and 7.31 +/- 0.13, 7.17 +/- 0.07, 7.08 +/- 0.08, and 7.07 +/- 0.12 in the epinephrine group. Despite a significant increase in myocardial and cerebral blood flow after epinephrine, PCO2 and pH in all blood samples were not different from those of the control group. (ABSTRACT TRUNCATED AT 250 WORDS)

Published results of dose-response effects of adrenergic drugs (epinephrine [E]) vary so much between studies because of differences in animal models and duration of ischemia before drug administration. In this investigation the effects of different doses of E on coronary perfusion pressure (CPP), left ventricular myocardial blood flow (MBF) and resuscitation success were compared during closed-chest cardiopulmonary resuscitation (CPR) after a 4-minute period of ventricular fibrillation in 28 pigs. MBF was measured during normal sinus rhythm using tracer microspheres. After 4 minutes of ventricular fibrillation CPR was performed with the use of a pneumatic piston compressor. After 4 minutes of mechanical measures only, the animals were randomly allocated into four groups of seven, receiving 0.015, 0.030, 0.045, and 0.090 mg/kg E intravenously respectively. MBF measurements were started 45 seconds after E administration; hemodynamic measurements after 90 seconds. Four minutes after the first administration, the same E dose was given before defibrillation. The CPP of animals given 0.015, 0.030, 0.045 and 0.090 mg/kg E were as follows: 16.3 +/- 6.1, 25.6 +/- 5.8, 33.2 +/- 8.4 and 30.4 +/- 6.3 mm Hg. The left ventricular MBF values were: 14 +/- 9, 27 +/- 11, 43 +/- 6, 46 +/- 10 mL/min/100 g. The differences between the groups receiving 0.015 and 0.045 mg/kg and between the groups receiving 0.015 mg/kg and 0.090 mg/kg were statistically significant (P less than .05). Resuscitation success was 14.3%, 42.9%, 100% and 86.7% respectively. A significant difference in resuscitation success was found only between 0.015 mg/kg and 0.045 mg/kg E.(ABSTRACT TRUNCATED AT 250 WORDS)

Norepinephrine, an alpha 1,2-beta 1,2-adrenergic agonist, seems to be an alternative to epinephrine, an alpha 1,2-beta 1,2-agonist, for restoration of spontaneous circulation in VF. We therefore studied the effect of epinephrine and norepinephrine on MDO2 and MVO2 using OCCM after five minutes of cardiopulmonary arrest in 21 pigs. After OCCM of three minutes, seven animals each received placebo (controls) or epinephrine (45 micrograms/kg) or norepinephrine (45 micrograms/kg). All drugs were given blindly. At 90 seconds after epinephrine or norepinephrine, mean arterial blood pressure was significantly higher than in the control group. Prior to cardiac arrest, MBF, measured with radioactive microspheres, was 193 +/- 30 ml/min/100 g. During CPR but before drug administration, MBF was 51 +/- 23 in the control group, 71 +/- 10 in the group with epinephrine, and 74 +/- 11 ml/min/100 g in the group with norepinephrine. At 90 seconds after epinephrine, MBF increased to 126 +/- 18 and after norepinephrine to 107 +/- 30 ml/min/100 g (p less than 0.05). Compared to OCCM alone, MDO2 increased from 9.6 +/- 1.7 to 17.1 +/- 3.2 ml/min/100 g after epinephrine and from 9.4 +/- 1.8 to 13.6 +/- 4.2 ml/min/100 g after norepinephrine (p less than 0.05). There was an increase in MVO2 from 4.0 +/- 1.5 to 9.4 +/- 3.0 ml/min/100 g after epinephrine (p less than 0.05), whereas MVO2 increased only from 4.2 +/- 0.8 to 5.1 +/- 2.0 ml/min/100 g after norepinephrine. Because epinephrine led to a greater increase in MVO2 than norepinephrine, the myocardial oxygen ER remained unchanged. The oxygen requirements of the fibrillating heart seemed to be increased via beta 2-adrenergic stimulation. In both the control and epinephrine-treated groups, only three of the seven animals could be successfully resuscitated, whereas all of the animals in the group with norepinephrine survived the 15-minute period of observation. In this model, norepinephrine, in contrast to epinephrine, improves the balance between MDO2 and MVO2 and eases restoration of spontaneous circulation.

The purpose of this study was to compare the efficacy of standard cardiopulmonary resuscitation and cardiopulmonary resuscitation with interposed abdominal compression for restoration of spontaneous circulation in an asphyxial and fibrillatory arrest model. Twenty-eight pigs weighing 19-27 kg were randomly allocated to two arrest groups. Each of these two groups was then subdivided into a treatment group and a control group resulting in four groups of seven pigs each. In the control groups standard cardiopulmonary resuscitation was performed with a pneumatically driven chest compressor at a rate of 80 beats per min. The animals' lungs were ventilated at a respiratory rate of 20 breaths per min independently of chest compression. In the treatment group, in addition to standard cardiopulmonary resuscitation, manual interposed abdominal compression was applied at the midabdomen in the second half of the relaxation phase using a blood pressure cuff to measure and standardize the compressions. Following asphyxial cardiac arrest of 3 min, none of the seven animals could be resuscitated with standard cardiopulmonary resuscitation, whereas all seven animals could be resuscitated with interposed abdominal compression and standard cardiopulmonary resuscitation after 240 +/- 84 s. Following fibrillatory cardiac arrest of 4 min, none of the seven animals that received standard cardiopulmonary resuscitation and countershocks could be resuscitated. In the group that received standard cardiopulmonary resuscitation and interposed abdominal compression spontaneous circulation was achieved in all animals in 244 +/- 117 s. End-diastolic arteriovenous pressure difference, which correlates with coronary blood flow, was significantly higher with interposed abdominal compression during resuscitation from both forms of cardiac arrest. The results of our study indicate that cardiopulmonary resuscitation with interposed abdominal compression in the second half of the relaxation phase improves diastolic arteriovenous pressure difference and resuscitation success in comparison with that following standard cardiopulmonary resuscitation. The use of interposed abdominal compression during basic cardiac life support should be investigated further in patients.

Three different resuscitation techniques were assessed by monitoring haemodynamic, respiratory, and cerebral parameters in 12 pigs of average body wt. (29 kg) following electrically induced cardiac arrest. All three techniques were carried out in randomised sequence, each for ten minutes, on each of the 12 animals. I = interposed ventilation and thoracic compression; S = simultaneous ventilation and thoracic compression; SA = simultaneous ventilation and thoracic compression plus abdominal binding 100 mm Hg. A compression rate of 60/min and ventilation rate of 12 min were used for each of the three techniques. 6 animals were ventilated with ZEEP for the whole of the 30 min observation period, the remainder with a PEEP of 5 cm H2O. In both ZEEP and PEEP groups the highest blood pressure and carotid artery flow rates were observed with the "SA" technique. PEEP ventilation and abdominal binding was found to be the most effective combination. Despite a rise in intracranial pressure, cerebral perfusion pressure rose when abdominal binding was applied. The CO2-production and arterio-venous oxygen difference of both ventilation groups were not significantly influenced by the different techniques. Even the technique "SA" did not markedly influence gas exchange or acid-base parameters. Despite an increase in the arterial base deficit and lactate levels during the course of resuscitation, the arterial pH did not fall below initial values because of the low paCO2. The positive effect of abdominal binding is a result of increased intrathoracic pressure, an increase in the effective circulating blood volume, and redistribution of blood flow.

The effect of epinephrine and norepinephrine on myocardial oxygen delivery and consumption during cardiopulmonary resuscitation using open cardiac massage after a 5-min period of electrically induced ventricular fibrillation was studied in 21 pigs with a mean body weight of 21 kg. Norepinephrine, like epinephrine, is a sympathomimetic agent with marked alpha- and beta-1-sympathomimetic activity, but the degree of beta-2-stimulation is less marked than that obtained with epinephrine. After mechanical measurements over 3 min (compression rate = 60/min), 7 animals received 10 ml physiological saline, 7 further animals, 45 micrograms/kg epinephrine, and the remaining 7 animals, 45 micrograms/kg norepinephrine. At 90 s and again at 5 min after the administration of epinephrine or norepinephrine, the mean arterial blood pressure was significantly higher than in the control group, while mean pulmonary artery pressure, central venous pressure and cardiac index were not significantly different. Total myocardial blood flow was only measured before the induction of cardiac arrest in the control group, where it was found be 193 +/- 30 ml/min/100 g. During the open cardiac massage but before the injection of catecholamines we found a myocardial blood flow of 51 +/- 23 in the control group, 71 +/- 10 in the epinephrine group, and 74 +/- 11 ml/min/100 g in the norepinephrine group. At 90 s after the injection, blood flow increased by 78% to 126 +/- 18, with epinephrine and by 45%, to 107 +/- 30 ml/min/100 g tissue with norepinephrine. At 5 min after administration of these catecholamines significant differences from the control group were present.(ABSTRACT TRUNCATED AT 250 WORDS)

Recent investigations concerning different techniques in respiratory and circulatory assistance during CPR lead to the following conclusions: Ventilation should start with two slow insufflations. To minimize ventilation pressure, insufflation should be performed in a pause between compressions for 1-1 1/2 seconds in two rescuer CPR. Due to the high arterio-venous gradient in pH and pCO2 during CPR, arterial blood gas analysis is only useful for evaluation for ventilatory efficiency and oxygenation. Acid-base dysregulation can better be determined in mixed and central venous blood. Blood flow during resuscitation seems to be generated by direct ventricular compression and thoracic pump mechanisms. Which mechanism is dominant seems to be interindividually different. Therefore a compression time of 50% of the compression cycle should be maintained.

A review of the literature indicates that the intravenous bolus dose of lidocaine should be reduced in all conditions where cardiac output is diminished. During external cardiac compression the cardiac output is only approximately 20-40% of the normal resting value. Various routes of drug administration are currently used during CPR. The routine use of a central venous line is not recommended as a first-line procedure for resuscitation. This route of administration is favored by some authors, however, because it is presumed to result in a more rapid onset of drug action and higher peak concentrations of the drugs used. The aim of this study was to determine the aortic plasma concentration of lidocaine after central venous as compared to peripheral venous administration under the conditions of external cardiac compression. Twelve pigs were allocated to two groups of 6 animals each using random numbers. Ventricular fibrillation was induced by applying an alternating current via two needle electrodes placed subcutaneously. Cardiac arrest was allowed to continue for a period of 1 min before mechanical measures were applied. Cardiac massage was carried out using a pneumatic piston device set to a compression rate of 80/min. Sixty seconds after mechanical CPR had been initiated, a bolus of 1.5 mg/kg lidocaine was given to 6 animals via a central venous line. The remaining 6 animals were treated with the same dose given into a vein of the earlobe. The 2% lidocaine solution was diluted to 20 ml with physiological saline in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of a bolus dose of epinephrine on hemodynamics, acid-base status and potassium during spontaneous circulation and cardiopulmonary resuscitation (CPR) was investigated in 24 pigs weighing 20-25 kg over a period of 10 min. In a study of 12 pigs in a stable hemodynamic condition, at the 1- and 2-min point after injection of epinephrine or saline the mean serum potassium concentration was significantly higher in the six animals given epinephrine (6.9 +/- 0.7 and 5.4 +/- 0.6 mmol/l, respectively) than in the six control animals (3.8 +/- 0.6 and 3.9 +/- 0.4 mmol/l, respectively). At the later points of observation (3, 4, 5 and 10 min after injection of either epinephrine or saline) no significant difference was found between the groups. Following 1 min of ventricular fibrillation 12 pigs were resuscitated by closed-chest CPR. Six of these animals received 45 micrograms/kg epinephrine (epinephrine group), the other six animals were given physiological saline (control group). Mean aortic diastolic pressure during the relaxation phase was significantly higher in the epinephrine group than in the control group. There was no difference in cardiac index or acid-base status between the groups. In the epinephrine group mean arterial serum potassium concentrations reached a peak value of 6.7 +/- 1.1 mmol/l at 3 min after injection, when they were significantly (P less than 0.05) higher than in the control group (4.4 +/- 0.5 mmol/l). At 5 and 10 min, the potassium levels sank to 5.9 +/- 0.9 and 5.6 +/- 0.8 mmol/l, respectively, in the epinephrine group, and were no longer significantly different from the control group.

Investigations on the delayed use of positive end-expiratory pressure (PEEP) following a standardized form of near drowning with 12.5 ml/kg body weight of either fresh or salt water were carried out on 14 anaesthetized and ventilated young pigs. After a 3-min period of apnoea the animals were ventilated with 100% oxygen and with either the same or an increased tidal volume, and a PEEP of 5 cmH2O delayed to 20 min, over a period of 2 h. In both fresh and salt water, initial values of PaO2 and AaDo2 were regained by the end of the period of observation when a delayed PEEP was applied. The intrapulmonary right to left shunt, which increased to 40% of the cardiac output, fell by a half within 10 min of beginning PEEP ventilation, initial values being regained after 120 min. During the period of apnoea the arterial partial pressure of carbon dioxide almost doubled, and, when the tidal volume remained unaltered, was still some 20-30% above initial values at the end of 2 h, despite the use of PEEP. Normal PaCO2 levels were achieved on increasing the tidal volume by a factor of 1.4. The larger tidal volume had no influence on either the degree of shunt or the PaO2. The effective compliance, which was considerably reduced after near drowning, increased again with the use of delayed PEEP ventilation. On beginning respiratory resuscitation there was an initial tachycardia and, despite a fall in stroke volume, an increase in mean arterial pressure and cardiac output because of the previous hypoxia. Only minimal cardiocirculatory changes, and no change in oxygen availability, occurred secondary to the use of PEEP.

Results obtained during animal investigations cannot be directly applied to patients because of the anatomical and physiological differences present. Experience has shown that cases of sudden cardiac arrest can only be effectively helped if cardiac massage and artificial ventilation are carried out as soon as possible, and that no sodium bicarbonate need be given when resuscitation measures are begun immediately, or very soon after arrest. In this situation it is better to use adrenaline only, in order to improve organ perfusion. The examples presented show that giving bicarbonate can alter potassium kinetics. Very low serum potassium concentrations are often measured during and following successful resuscitation, and giving too large an amount of buffer solution can worsen this hypokalaemia and lead to a further arrest. The infusion of sodium bicarbonate and the rapid increase in blood sugar levels during resuscitation can lead to a marked rise in serum osmolality which in turn can jeopardize the return of cerebral function. Because in the presence of reduced cerebral perfusion, high blood glucose levels increase the degree of cerebral lactacidosis blood glucose levels should be measured and corrected as necessary.

Investigations on the delayed use of PEEP following a standardized form of near drowning with 12.5 ml/kg body weight of either fresh or salt water were carried out on 14 anaesthetized and ventilated young pigs. After a 3 min period of apnoea the animals were ventilated with 100% oxygen and with either the same or an increased tidal volume, and a PEEP of 5 cm H2O delayed to 20 min, over a period of 2 h. In both fresh and salt water, initial values of paO2 and AaDO2 were regained by the end of the period of observation when a delayed PEEP was applied. The intrapulmonary right to left shunt, which increased to 40% of the cardiac output, fell by a half within 10 min of beginning PEEP ventilation, initial values being regained at 120 min. During the period of apnoea the arterial partial pressure of carbon dioxide almost doubled, and, when the tidal volume remained unaltered, was still some 20-30% above initial values at the end of 2 h despite the use of PEEP. Normal paCO2 levels were achieved on increasing the tidal volume by a factor of 1.4. The larger tidal volume had no influence on either the degree of shunt or the paO2. The effective compliance, which was considerably reduced after near drowning, increased again with the use of delayed PEEP ventilation. On beginning respiratory resuscitation there was an initial tachycardia and, despite a fall in stroke volume, an increase in mean arterial pressure and cardiac output because of the previous hypoxia. Only minimal cardio circulatory changes, and no change in oxygen availability, occurred secondary to the use of PEEP.

One minute following electrically induced ventricular fibrillation, 12 anaesthetized pigs (hybrids between German and Belgian pedigree swine of 29 kg average body weight) were resuscitated for 30 min with a mechanical thorax compressor and ventilator. Six animals were given 1 mval sodium bicarbonate per kilogram body weight via a central venous line during the first ten minutes of resuscitation, and then 0.5 mval/kg body weight during both of the remaining ten minute intervals. The remaining 6 animals served as control group. In the control group constant volume ventilation led to a fall in the arterial partial pressure of CO2 because perfusion was diminished in relation to ventilation and despite the slowly developing metabolic acidosis this initially led to an increase in pH. At the end of the period of observation an arterial base deficit of 10 mmol/l was measured. Infusion of sodium bicarbonate led to a metabolic alkalosis and to an arterial base excess which at 10 min reached a maximum value of 13.8 mmol/l. In the bicarbonate group serum osmolality rose as a result of the sodium application from 293-334 mosm/l. In contrast, the osmolality of the control group only rose to 309 mosm/l.

During external cardiac massage and after restoration of spontaneous circulation, the arterial and central venous blood gas status of ten patients was determined. During cardiopulmonary resuscitation the median arterial pH value was 7.29 and the median central-venous pH value was 7.16. The low central-venous pH during resuscitation was probably caused by the high partial pressure of carbon dioxide, because no significant difference between arterial and central-venous base deficit was found. The arteriovenous pH and carbon dioxide gradients were significantly lower after spontaneous circulation had been restored. The arterial pH does not parallel the marked fall in central venous pH, and therefore only partly indicates acid-base changes during resuscitation. On the other hand, a central-venous blood gas status not only indicates the degree of metabolic acidosis present, but also the "respiratory" acidosis that in turn is a measure of the severity of intracellular acidosis.

The effectiveness of epinephrine and dopamine for restoring spontaneous circulation after asphyxial or fibrillatory cardiac arrest was compared using a porcine model. Asphyxial arrest: 7 animals received 45 micrograms/kg epinephrine, 7 animals 2.5 mg/kg dopamine, the remaining 7 animals received no drug treatment. All 7 animals given epinephrine could be resuscitated after 174 +/- 53 s, spontaneous circulation could be restored in only 3 of 7 animals given dopamine after 487 +/- 63 s and in none of the control animals could spontaneous circulation be established. Ventricular fibrillation: 7 animals were defibrillated without either mechanical measures or drug therapy. The following doses were given before defibrillation and after starting mechanical measures to separate groups of 7 animals each: 45 micrograms/kg epinephrine, 2.5 mg/kg dopamine, or no drug therapy. In the absence of either drug or mechanical measures and with mechanical measures only, spontaneous circulation could not be established in any of the cases. After administration of epinephrine, defibrillation and restoration of spontaneous circulation was achieved in 6 of 7 animals in 667 +/- 216 s, with dopamine, all the animals could be successfully resuscitated in the shorter time of 174 +/- 85 s. Epinephrine was found to be superior to dopamine in the treatment of asphyxial arrest whereas dopamine was found to be better in the management of ventricular fibrillation, probably by improving the balance between myocardial oxygen supply and demand.